PubMed Health⌕ Search

Biomedical subjects

K Hanazaki

Publications and source records attributed to K Hanazaki.

At least 55 records · Page 3Linked to original sources

Gas-forming liver abscess after transcatheter arterial embolization for hepatocellular carcinoma: report of a case.

A case of a gas-forming liver abscess developing after transcatheter arterial embolization for recurrent hepatocellular carcinoma (HCC) in a 65-year-old man is presented herein. He was admitted to hospital with fever and jaundice, following which ultrasonography (US) and computed tomography revealed a gas-containing abscess in the posterior segment of the hepatic lobe with multiple HCC. Percutaneous transhepatic drainage was performed using US. Antibiotics which were sensitive to the Escherichia coli bacteria detected in the abscess were administered both intravenously and through the drainage tube into the abscess. Four months later, the abscess had diminished and the patient was discharged after receiving percutaneous ultrasonographically guided ethanol injection therapy for the recurrent HCC.

Carcinoma, Hepatocellular↗

Metabolism of insulin and glucagon in liver and pancreas in dogs with obstructive jaundice.

Insulin and glucagon metabolism in the pancreas with obstructive jaundice caused by complete ligation of the common bile duct and in the cholestatic liver caused by hepatic duct ligation was evaluated experimentally using dogs. The isolated perfused pancreas in obstructive jaundiced dogs, which showed a low insulin response in the peripheral blood after intravenous glucose administration, revealed depression of insulin production and no change of glucagon production in response to cholecystokinin octapeptide. The extraction of insulin in the cholestatic lobe of the liver was decreased compared with that in the noncholestatic lobe. The extraction of glucagon, on the other hand, in the cholestatic lobe and in the noncholestatic lobe showed no significant difference. So the imbalance of glucose metabolism in obstructive jaundice does not depend on the enhanced extraction of insulin in the liver, but on the depression of insulin production in the pancreas.

Animals↗

Enhanced sensitivity of pancreatic cells to cholecystokinin octapeptide in obstructive jaundice.

Exocrine function of the pancreas in obstructive jaundice was examined using dogs. Jaundice induced by choledochal ligation over 3 weeks showed pancreatic hypersecretion in response to cholecystokinin octapeptide (CCK-8) stimulation. To clarify the mechanism of pancreatic hypersecretion in obstructive jaundice, three experiments were undertaken. In a perfusion experiment performed on isolated pancreas, hypersecretion in obstructive jaundice was observed in response to CCK-8 stimulation. An incubation experiment showed an increase in secretion in response to CCK-8 stimulation in a dose-dependent manner, producing a greater increase in dogs with obstructive jaundice than in controls, despite the fact that basal secretion in both groups was the same. This would suggest that at least one of the mechanisms of pancreatic hypersecretion in obstructive jaundice may be related to the degree of sensitivity of acinar cells to CCK-8. In morphological observation of acinar cells by electron microscopy, the average number of zymogen granules and total granular area per unit of cytoplasm in both groups before and after stimulation with CCK-8 were compared. There was no difference between the groups before stimulation. Following stimulation, values for the control group decreased but appeared to increase in the jaundiced pancreas. These results strongly suggest that pancreatic acinar cells in obstructive jaundice may retain their secretory potential after stimulation for 60 min, though the potential in nonjaundiced pancreatic acinar cells may decrease after stimulation.

Animals↗

Effects of parathyroid hormone on pancreatic exocrine secretion.

The role of parathyroid hormone (PTH) and calcium on pancreatic exocrine secretion were observed using sham-operated and parathyroidectomized dogs. First, exocrine secretion of the pancreas stimulated with secretin and cholecystokinin octapeptide (CCK-8) was examined in vivo 3 weeks after parathyroidectomy. Secondly, perfusion experiments of isolated pancreas in the sham-operated and parathyroidectomized dogs were examined. In one experiment, volume of pancreatic juice and bicarbonate output, but not amylase output, was decreased in the parathyroidectomized dogs compared with those in the sham-operated dogs; no participation of calcium in exocrine secretion was revealed. In another experiment, high doses of PTH evoked increases of pancreatic juice and bicarbonate output without changing amylase output; as before, no participation of calcium in the exocrine secretion was observed. We conclude that (a) PTH increases volume of pancreatic juice and bicarbonate output, and (b) pancreatic exocrine secretion is modified by direct effect of PTH, and the pancreatic ductular cells, not the acinar cells, are the target for PTH.

Amylases↗

[Assessment for protective effects of CoQ10, PGE1 and TXA2 receptor antagonist (ONO-3708) on warm ischemic liver].

Metabolic disturbances in the canine liver during warm ischemia by Pringle's method for 60 minutes and the role of Coenzyme Q10 (CoQ10), Prostaglandin E1 (PGE1) and ONO-3708, TXA2 receptor antagonist, were studied. Mongrel dogs were divided into five groups; control group, group of liver ischemia without drugs, groups of liver ischemia with CoQ10, PGE1 and ONO-3708 pretreatment. Metabolic rates of PGI2, TXA2, insulin, glucagon and glucose and production of lipid peroxides in the five groups were measured at the points before Pringle's procedure, 5 minutes, 60 minutes and 120 minutes after declamping. In the group of ischemia without drug administration, the hepatic metabolism of PGI2, TXA2, insulin and glucose were decreased after declamping. The metabolism of glucagon, however, was not disturbed by warm ischemia. The production of lipid peroxides increased at 5 minutes after declamping. In the groups of CoQ10, PGE1 and ONO-3708 pretreatment, changes of PGI2, TXA2 and insulin metabolism in the liver were improved, and an increased production of lipid peroxides by warm ischemia was normalized. This study suggests that CoQ10, PGE1 and ONO-3708 protect liver damage by warm ischemia as results of improvement of metabolic disturbances of PGI2, TXA2, insulin and suppression of lipid peroxides production.

Alprostadil↗

Enhanced production of endogenous prostaglandin in obstructive jaundiced pancreas in dogs.

Endogenous pancreatic prostaglandin production in control and obstructive jaundice was investigated using isolated and perfused dog pancreas. In both groups, spontaneous production of prostaglandin E2 and prostaglandin I2 was recorded, and the levels did not change in both groups. The production of both prostaglandins in jaundice, however, was higher than that in the control on stimulation by 8 x 10(-11) mol of cholecystokinin-octapeptide. Amylase release with cholecystokinin-octapeptide at an amount of 8 x 10(-11) mol in jaundice was higher than in the control. The amylase release in both groups, however, showed further elevation on indomethacin pretreatment. On incubation of pancreatic dispersed cells in both groups, prostaglandin production in jaundiced cells was higher than that in control cells. These data showed that enhanced endogenous prostaglandin in obstructive jaundice might be caused by the characteristic change of pancreatic cells, which increased susceptibility to cholecystokinin-octapeptide because of long-term exposure to abnormal blood components, and enhanced prostaglandins might act as a cytoprotector of acinar cells in the pancreas damaged by cholecystokinin-octapeptide administration.

6-Ketoprostaglandin F1 alpha↗

Involvement of endogenous prostaglandins in pancreatic endocrine and exocrine secretion in dog pancreas.

The involvement of endogenous prostaglandins (PGs) in pancreatic endocrine and exocrine secretion was investigated, using the isolated and perfused dog pancreas. Spontaneous production of both PGE2 and 6-keto-PGF1 alpha was recorded in venous effluent. Prostaglandin production increased following stimulation with both 10 x 10(-11) and 20 x 10(-11) mol of CCK-8, but was not affected by a 5 x 10(-11) mol infusion. Insulin, glucagon, and amylase release was stimulated by 10 x 10(-11) mol of CCK-8. Indomethacin pretreatment with 10 mg/kg totally abolished endogenous PG production, but failed to suppress an insulin and glucagon response. On the other hand, an amylase response was accelerated by indomethacin pretreatment. Although low dose CCK-8 failed to stimulate endogenous prostaglandin production, a brisk exocrine secretion was not suppressed by indomethacin pretreatment. From the above results, we conclude that endogenous PGs do not appear to play an important role in pancreatic endocrine and exocrine secretion, but might have a cytoprotective effect on the pancreatic acinar cells damaged by CCK-8.

Amylases↗

Idiopathic saccular aneurysm of the azygos vein.

Idiopathic saccular aneurysm of the azygos vein is a rare condition. We report the case of a 52-year-old man with saccular aneurysm of the azygos vein who underwent surgical resection. Preoperative dynamic computed tomography revealed strong and rapid enhancement of the chest mass. Magnetic resonance imaging showed a thoracic tumor with low signal intensity on the T1-weighted image and coexistence of low and high signal intensity on the T2-weighted image. Intraoperative findings showed cystic dilatation of the azygos vein. Although an accurate preoperative diagnosis of saccular azygos vein aneurysm is difficult, especially differential diagnosis between this anomaly and mediastinal tumors, a markedly enhanced mass shown by dynamic computed tomography was useful for the preoperative diagnosis of this anomaly.

Azygos Vein↗

Hepatic arterial infusion chemotherapy of cisplatin for biliary cystadenocarcinoma.

Biliary cystadenocarcinoma is a rare tumor which has a better prognosis after complete surgical removal. However, since there is no other effective therapeutic option instead of surgery, the prognosis is very poor if surgical resection is impossible. We report the case of a 78 year-old woman who was treated only by hepatic arterial infusion (HAI) chemotherapy of cisplatin (85 mg) because liver functional reserve was too bad to perform a major hepatectomy. Huge biliary cystadenocarcinoma occupying the right lobe of the liver measuring 12 cm in size before chemotherapy was drastically decreased to 2 cm in size 8 months after chemotherapy. Although she had abdominal pain and anorexia before chemotherapy, she is doing well and has no complaints 9 months after chemotherapy. In conclusion, an effective therapy may be possible using hepatic arterial infusion chemotherapy of cisplatin in patients with biliary cystadenocarcinoma for whom surgical treatment is not suitable.

Aged↗

Histochemical study of vascular endothelial growth factor in squamous cell carcinoma of the esophagus.

BACKGROUND/AIMS: Vascular endothelial growth factor (VEGF) plays a key role in tumor angiogenesis. The aim of this study was to clarify the significance of VEGF expression in esophageal squamous cell carcinoma (SCC). METHODOLOGY: Tissues samples were taken from 52 patients with esophageal SCC after surgery. VEGF expression in these SCCs was examined immunohistochemically. Microvessels in the tumor stained for Factor VIII-related antigen were counted. Ki-67 antigen as a proliferative marker was immunostained with MIB-1, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick end labeling was performed for the evaluation of apoptosis. Ki-67 labeling index (LI) and apoptotic index were then calculated. RESULTS: VEGF expression was observed in 30 of the patients (57.7%). The microvessel count was significantly higher (p = 0.007), and the apoptotic index was significantly lower (p < 0.0001) in the SCC with VEGF expression than in the SCC without it, but no significant difference was observed in the Ki-67 LI between these groups. There was an inverse correlation between the microvessel count and the apoptotic index (p = 0.007). In the clinicopathologic factors, histologic venous invasion of cancer cells (p = 0.039) and lymph node metastasis (p = 0.049) were significantly correlated with VEGF expression. The survival rate after curative surgery was better in the patients without VEGF expression (p < 0.05), and distant organ metastasis after surgery was frequently observed in the patients with VEGF expression (p = 0.023). CONCLUSIONS: These results suggest that VEGF expression is associated with angiogenesis in esophageal SCC, and may be a prognostic factor in patients with esophageal SCC. Furthermore, apoptosis may be influenced by angiogenesis in esophageal SCC.

Aged↗

Risk factors associated with intra-operative blood loss in hepatectomized patients with giant cavernous hemangioma of the liver.

BACKGROUND/AIMS: The aim of this study was to clarify risk factors associated with intra-operative blood loss in hepatectomized patients with giant cavernous hemangioma (GCH) of the liver. METHODOLOGY: Twenty patients with GCH of the liver were treated by hepatectomy. Eleven patients with intra-operative blood loss > 2000 ml (mean: 7145 +/- 7080 m; Group 1) were reviewed retrospectively and compared to 9 patients with intra-operative hemorrhage < 2000 ml (mean: 918 +/- 429 ml; Group 2). RESULTS: Although there were no significant differences in pre-operative AST, ALT, and ICG-15 or fibrinogen and platelets between the two groups, pre-operative total bilirubin and fibrin degradation product (FDP) in Group 1 was significantly higher than in Group 2. Mean operation time and intra-operative blood transfusion in Group 1 versus Group 2 were 433 min vs. 213 min (p < 0.0001) and 3036 ml vs. 422 ml (p = 0.0072), respectively. The weight of resected liver (r = 0.821, p < 0.0001), maximum diameter of tumor (r = 0.782, p < 0.0001) and operation time (r = 0.748, p < 0.0001) were the most highly correlated with intra-operative blood loss, followed by pre-operative total bilirubin (r = 0.605, p = 0.0038), FDP level (r = 0.576, p = 0.0068) and intra-operative blood transfusion (r = 0.561, p = 0.0089). CONCLUSIONS: These findings suggest that pre-operative management to reduce the tumor size, total bilirubin and FDP levels may be essential to minimize intra-operative hemorrhage and blood transfusion.

Adult↗

Post-operative chemotherapy in non-curative gastrectomy for advanced gastric cancer.

BACKGROUND/AIMS: The definitive effects of post-operative chemotherapy for prolonging survival in patients with non-curative gastrectomy for advanced gastric cancer have not been established. METHODOLOGY: Eighty-three patients with advanced gastric cancer who underwent non-curative gastrectomy were divided into 49 patients with post-operative chemotherapy (chemotherapy group) and 34 patients without post-operative chemotherapy (control group). Chemotherapy regimens were as follows: oral 5-fluorouracil (5-FU) alone (n = 22), intravenous mitomycin (MMC) plus 5-FU (n = 20), intravenous methotrexate (MTX) plus 5-FU (n = 3), intravenous cisplatin plus 5-FU (n = 2), and hepatic arterial infusion of 5-FU plus oral 5-FU (n = 2). No prior chemotherapy or radiation therapy was given. RESULTS: Although the age in the control group (mean: 71.9 years) was significantly older than in the chemotherapy group (mean: 66.1 years), there were no significant differences in the other clinical and pathological background data between the two groups. The 1-year survival rate in the chemotherapy group (71.4%) was significantly higher than in the control group (50.0%). However, the 3-year and 5-year survival rates did not significantly differ in the chemotherapy group versus the control group, 30.6% vs. 32.4% and 24.5% vs. 32.4%, respectively. Although a significant difference did not exist between the two groups, median survival after operation in the chemotherapy group (20.5 months) was longer than that in the control group (16.2 months). Furthermore, median survival of patients with peritoneal dissemination in the chemotherapy group (16.4 months) was significantly longer than that in the control group (7.7 months). CONCLUSIONS: Post-operative chemotherapy may contribute to prolonged survival in patients with non-curable advanced gastric cancer, even when patients had peritoneal dissemination. However, the long-term survival rate was not improved by post-operative chemotherapy. More aggressive chemotherapy may be needed to improve the long-term prognosis for such patients.

Adenocarcinoma↗

Efficacy of extended lymphadenectomy in the noncurative gastrectomy for advanced gastric cancer.

BACKGROUND/AIMS: We retrospectively analyzed clinicopathologic data on 83 patients with advanced gastric cancer who underwent noncurative gastrectomy, with respect to the relation between the extent of lymphadenectomy and survival benefit. METHODOLOGY: These 83 patients were divided into 44 patients with limited or simple lymph node dissection (D0 in 14 and D1 in 30: Group A) and 39 patients with extended lymph node dissection (D2: Group B). RESULTS: The 1-year survival rate in Group B (82.1%) was significantly higher than in Group A (49.0%). However, the 3-year and 5-year survival rates did not significantly differ between Group A versus Group B, 39.7% versus 25.7% and 39.7% versus 20.5%, respectively. Median survival time after surgery with and without distant metastasis in Group B (21.5 months) was longer than in Group A (16.4 months), although not significant. CONCLUSIONS: While gastrectomy with extended lymphadenectomy did not contribute to improve long-term survival in patients with noncurable advanced gastric cancer, the utility of extended lymph node dissections may be relevant to improved locoregional control, at least in the prognosis within 1 year after surgery. Not only extended lymphadenectomy but also aggressive chemotherapy may be needed to improve the long-term survival for such patients.

Aged↗

Synchronous gastric cancer associated with hepatocellular carcinoma: a study of 10 patients.

BACKGROUND/AIMS: Little information regarding synchronous gastric cancer (GC) associated with hepatocellular carcinoma (HCC) is available. The aim of this study was to clarify the clinicopathologic features of synchronous GC associated with HCC, and we also discuss the diagnostic and therapeutic issues regarding them. METHODOLOGY: In a series of 396 patients with GC and 340 patients with HCC, we investigated the clinicopathologic features of the patients with synchronous GC associated with HCC (HCC group; n=10). They were compared to the patients with resected GC without HCC (non-HCC group) which was divided into 2 groups: with chronic hepatic disease (CHD: CHD group; n=15) and without CHD (Control group; n=345). RESULTS: The HCC group consisted of 10 of the 396 patients with GC (2.6%), and of 340 with HCC (2.9%). Eight node-negative early GC and 2 advanced GC cases were observed in the HCC group. Nine of these GC (90%) were well-differentiated adenocarcinoma. The tumor sizes of the HCC group were significantly smaller than those of the control group (p<0.05). The incidences of intestinal type and early GC in the HCC group were significantly higher than those in the control group, (p<0.05). However, there were no significant differences in any parameters between the HCC group and CHD group. With regard to early GC, there were no significant differences in any parameters, excluding the site of GC in the CHD group, between the HCC group and non-HCC group. Eight in the HCC group were surgically resected, and the post-operative period of these patients was uneventful. Although there were no significant differences in survival after surgery among the 3 groups, the survival of the patients with early GC in the HCC group was significantly worse than that in the control group (p<0.01). CONCLUSIONS: The clinicopathologic features of synchronous GC associated with HCC are not very aggressive in most patients probably because of the early detection, and those of early GC with HCC appeared to resemble that of GC with CHD. Since early GC may not influence the clinical outcome of HCC patients, limited gastric resection can be recommended even when curative surgery for HCC is performed. By contrast, when advanced GC is present, curative gastrectomy with lymphadenectomy would be advisable to improve the long-term survival.

Adenocarcinoma↗

Hepatic function immediately after hepatectomy as a significant risk factor for early recurrence in hepatocellular carcinoma.

BACKGROUND/AIMS: The aim of this study was to clarify the significant risk factors as they relate to early recurrence after hepatectomy in cirrhotic patients with hepatocellular carcinoma (HCC). METHODOLOGY: We retrospectively investigated 42 cirrhotic patients undergoing hepatectomy for a single HCC. We compared the clinicopathologic features of 14 patients with early intrahepatic recurrence (recurrence was detected within 1 year after hepatic resection; Group 1) with 28 patients without recurrence or with late intrahepatic recurrence (recurrence was confirmed more than 1 year after hepatic resection; Group 2). RESULTS: There were no significant differences in the pre-operative and intra-operative clinical background data or pathological data between the 2 groups. Regarding recurrence pattern, although not significant, the incidence of intrahepatic metastasis in Group 1 (85.7%) was higher than in Group 2 (50.0%). Maximum values of total bilirubin and albumin within 7 days after hepatectomy for patients in Group 2 were significantly better than those in Group 1. Aspatate aminotransferase (AST) and alanine aminotransferase (ALT) immediately after hepatectomy in Group 1 were also higher than in Group 2, although statistically insignificant. The overall 1-year and 3-year survival rates between Group 1 versus Group 2 were 85.7% versus 100% (p < 0.01) and 57.2% versus 90.0% (p < 0.01), respectively. CONCLUSIONS: Hepatic functional damage immediately after hepatectomy is as significant risk factor for early intrahepatic recurrence in cirrhotic HCC. Careful perioperative management of hepatic function may therefore be important in preventing early recurrence and prolonging survival.

Alanine Transaminase↗

Surgical outcome in cirrhotic patients with hepatitis C-related hepatocellular carcinoma.

BACKGROUND/AIMS: The aim of this study was to clarify the surgical outcome in cirrhotic patients with hepatitis C-related hepatocellular carcinoma (HCC). METHODOLOGY: The surgical outcome of 26 HCVAb-positive cirrhotic patients with hepatitis C antibody (the C-related HCC group) and 18 HCVAb-negative cirrhotic patients with (the non-C-related HCC group) undergoing hepatectomy for HCC were compared. The C-related HCC group was HCVAb[+], HBsAg[-] for hepatitis B surface antigen in 25 patients and HCVAb[+], HBsAg[+] in 1, and the non C-related HCC group was HCVAb[-], HBsAg[+] in 15 and HCVAb[-], HBsAg[-] in 3. RESULTS: Preoperative aspartate and alanine aminotransferase in the C-related HCC group were significantly (P < 0.01) higher than in the non-C-related HCC group. There were no significant differences in the operative method, intraoperative blood loss and weight of resected liver or pathological data between the 2 groups. In the recurrence pattern, the incidence of multicentric occurrence in the C-related HCC group (53.3%) was significantly (P < 0.05) higher than in the non-C-related HCC group (7.7%). The mortality rate in both groups was 0% and no operative death was encountered. The crude survival and disease-free survival rates at 3 years were similar: 80.8% and 57.7% in the C-related HCC group and 77.8% and 55.6% in the non-C-related HCC group, respectively. CONCLUSIONS: Although surgically treated cirrhotic patients with C-related HCC showed worse preoperative hepatitis status and a higher incidence of recurrence due to multicentricity compared with non-C-related HCC, the mortality and prognosis of patients with C-related HCC did not differ from that of non-C-related HCC. The indication of hepatic resection and consideration for the high incidence of postoperative multicentric occurrence in the patients with C-related HCC should therefore be more careful than in patients with non-C-related HCC.

Carcinoma, Hepatocellular↗

Effects of prostaglandin E1 administration during hepatectomy for cirrhotic hepatocellular carcinoma.

BACKGROUND/AIMS: Prostaglandin E1 has been used in hepatectomy based on a few limited clinical studies suggesting that PGE1 improves liver function. The aim of this study was to evaluate the effects of PGE1 administration during hepatectomy for cirrhotic hepatocellular carcinoma. METHODOLOGY: Forty-three patients undergoing hepatectomy for cirrhotic hepatocellular carcinoma were divided into 2 groups: hepatectomy with Prostaglandin E1 treatment (PG group; n = 19) and without Prostaglandin E1 treatment (control group; n = 24). Prostaglandin E1 (0.02-0.07 microgram/kg/min) was administered intravenously from beginning to end of surgery in the PG group. RESULTS: There were no significant differences between groups with respect to age, gender, preoperative liver and renal function, or intraoperative variables such as blood loss, weight of resected liver and total clamping time by the Pringle maneuver. No patient had severe postoperative complications. Initial postoperative maximum concentrations of serum total bilirubin, creatinine, and blood urea nitrogen in the PG group were significantly lower than those in the control group. CONCLUSIONS: Prostaglandin E1 administration during hepatectomy for cirrhotic heptocellular carcinoma resulted in improved renal and hepatic function.

Aged↗